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Brain hemorrhage Vs infarction
in CT and MRI
Thamir Diab Alotaify
4th year – medical student
NBU – medical college
Objectives
•
•
•
•
•

Types of cerebral strokes and etiology
CT and MRI in cerebral hemorrhage
CT and MRI in cerebral infarction
4-min Vedio for learning purpose
Conclusion
Intracrainial hemorrhage
Def / active bleeding inside the cranial cavity
Types :
- Epideural
- Subdeural
- Subarachnoid
- Intracerebral (intraparnchymal)
- Intraventricular
Etiology
• Generally most common cause of ICHs are
traumatic causes
• And the most common cause of such traumas
are RTAs
• Always it is nessery to evaluate the head and
neck after RTAs
Clinically +++ radiologically
Even if the patient is Asymptomaic(lucid interval )
CT and MRI in ICH
• CT scan is the modality of choice in traumatic
head injuries ( in ER)
• Why ?
- Rapid
- It can shows the bone status
- It can detect the early onset of hemorrhge
• So the CT good for 3 Bs
-Blood
-Brain
-Bone
Stages of brain hemorrhage in CT
• Acute : hyperdense
• Sub acute : isodense
• Chronic : hypodense
CT appearance of hemorrhage.
Serial CT scans
of right thalamic hematoma. (A)
Acute ICH in the
right thalamus with mean
attenuation 65 HU. (B) CT
performed 8 days later than (A);
the periphery of
the hematoma is now isodense to
the brain while
the center of the hematoma has
mean attenuation
45 HU. (C) CT performed 13 days
later than (A) shows
continued evolution of the
hematoma with decreasing
attenuation. (D) CT performed 5
months later
than (A) shows a small area of
encephalomalacia in
ICH in MRI
• MRI is not a best choice for urgent diagnosis ,
it takes time and may be not available , and
not good for bone status (not usefull in acute
head injury )
• But it is the best modality for brain
paranchymal assessment ( infarcts,
demyelinatind dis , Tumors )
Brain infarction
•
•
•
•
•

Def/ necrosis of brain tissue due to many causes
types : (global , focal)
Most common cause : ischemia
Other causes :
Metabolic : hypoglycemia
Toxic : drugs
Cerebral infarction it can be detected in both CT
& MRI
• CT may appear normal in hyperacute state ( <3h)
• MRI can detect small infarction at the moment
Cerebral infarction on CT
•
•
•
•
-

Hyperacute : before 3houres of onset ..normal
Early acute (4-6) :
Chronic : (>3days)
Dense MCA sign
Obscuration of the lenticular nucleus
-Well demarcated hypodensity
insular ribbon Sign
Simillar density to CSF
Late acute :
--ve mass effect (pulled midline)
-Dilataion of ventricles
Low density basalganglia
(Encephalomalacia )
sulcal effacement
Subacute :
Increasing mass effect
Wedge-shaped low density area involving gray and white matter
Possible hemorrhagic transformation
Early acute (3-6 )
MCA
sign
Subacute cerebral infarction
Marked ill defined
hypodense area
involving most of the
RT cerebral
hemisphere and
shifting the midline
Chronic cerebral infarction
Massive Hypodense area in
LT cerebral hemispher
Simillar density of CSF
+ ipsilateral widening of
lateral ventricle
Cerebral infarction in MRI
+ve DWI
Imaging Findings of Stroke:
Acute Stroke (up to 7 days)

• MR imaging of the brain is far more sensitive than CT imaging to recognize acute
infarction.
• Diffusion wtd. pulse sequence (DW imaging) is the most sensitive MR sequence to
demonstrate stroke. This sequence is sensitive to restricted diffusion within the cell from
stroke-induced cytotoxic edema and the region of acute stroke is seen as an area of bright
signal on DWI Cytotoxic edema can occur immediately after the initial insult thus DWI
images can reveal, the area of acute infarct immediately after the insult.
• Intravascular contrast enhancement, another sign of early stroke (Figure 1f).
• Sulcal effacement, gyral edema (Fig. 5b), loss of gray-white matter interface can occur
within 12 hours of stroke.
• Parenchymal contrast enhancement (Fig. 6d), mass effect (Fig. 4b) and hemorrhage can
occur within 1-7 days of insult.
Subacute infarct: (1 week to 8 weeks)
• Contrast enhancement slowly decreases in time but can persist for 8 weeks, with
decreasing mass effect and abnormal signal intensity:

Old Infarct:
•Focal area of encephalomalacia
•Porencephalic dilatation of adjacent ventricle.
• Residual old blood products may be present.
conclusion
• There are sequence of events in cerebral
strokes :
- Hyperacute
- Acute
- Subacute
- Chronic
• CT is best for hemorrhagic
• MRI is best to detect the ischemic at the onset
Radiology of Brain hemorrhage vs infarction

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Radiology of Brain hemorrhage vs infarction

  • 1. Brain hemorrhage Vs infarction in CT and MRI Thamir Diab Alotaify 4th year – medical student NBU – medical college
  • 2. Objectives • • • • • Types of cerebral strokes and etiology CT and MRI in cerebral hemorrhage CT and MRI in cerebral infarction 4-min Vedio for learning purpose Conclusion
  • 3. Intracrainial hemorrhage Def / active bleeding inside the cranial cavity Types : - Epideural - Subdeural - Subarachnoid - Intracerebral (intraparnchymal) - Intraventricular
  • 4. Etiology • Generally most common cause of ICHs are traumatic causes • And the most common cause of such traumas are RTAs • Always it is nessery to evaluate the head and neck after RTAs Clinically +++ radiologically Even if the patient is Asymptomaic(lucid interval )
  • 5. CT and MRI in ICH • CT scan is the modality of choice in traumatic head injuries ( in ER) • Why ? - Rapid - It can shows the bone status - It can detect the early onset of hemorrhge • So the CT good for 3 Bs -Blood -Brain -Bone
  • 6. Stages of brain hemorrhage in CT • Acute : hyperdense • Sub acute : isodense • Chronic : hypodense
  • 7. CT appearance of hemorrhage. Serial CT scans of right thalamic hematoma. (A) Acute ICH in the right thalamus with mean attenuation 65 HU. (B) CT performed 8 days later than (A); the periphery of the hematoma is now isodense to the brain while the center of the hematoma has mean attenuation 45 HU. (C) CT performed 13 days later than (A) shows continued evolution of the hematoma with decreasing attenuation. (D) CT performed 5 months later than (A) shows a small area of encephalomalacia in
  • 8. ICH in MRI • MRI is not a best choice for urgent diagnosis , it takes time and may be not available , and not good for bone status (not usefull in acute head injury ) • But it is the best modality for brain paranchymal assessment ( infarcts, demyelinatind dis , Tumors )
  • 9.
  • 10.
  • 11. Brain infarction • • • • • Def/ necrosis of brain tissue due to many causes types : (global , focal) Most common cause : ischemia Other causes : Metabolic : hypoglycemia Toxic : drugs Cerebral infarction it can be detected in both CT & MRI • CT may appear normal in hyperacute state ( <3h) • MRI can detect small infarction at the moment
  • 12. Cerebral infarction on CT • • • • - Hyperacute : before 3houres of onset ..normal Early acute (4-6) : Chronic : (>3days) Dense MCA sign Obscuration of the lenticular nucleus -Well demarcated hypodensity insular ribbon Sign Simillar density to CSF Late acute : --ve mass effect (pulled midline) -Dilataion of ventricles Low density basalganglia (Encephalomalacia ) sulcal effacement Subacute : Increasing mass effect Wedge-shaped low density area involving gray and white matter Possible hemorrhagic transformation
  • 13. Early acute (3-6 ) MCA sign
  • 14. Subacute cerebral infarction Marked ill defined hypodense area involving most of the RT cerebral hemisphere and shifting the midline
  • 15. Chronic cerebral infarction Massive Hypodense area in LT cerebral hemispher Simillar density of CSF + ipsilateral widening of lateral ventricle
  • 16. Cerebral infarction in MRI +ve DWI
  • 17. Imaging Findings of Stroke: Acute Stroke (up to 7 days) • MR imaging of the brain is far more sensitive than CT imaging to recognize acute infarction. • Diffusion wtd. pulse sequence (DW imaging) is the most sensitive MR sequence to demonstrate stroke. This sequence is sensitive to restricted diffusion within the cell from stroke-induced cytotoxic edema and the region of acute stroke is seen as an area of bright signal on DWI Cytotoxic edema can occur immediately after the initial insult thus DWI images can reveal, the area of acute infarct immediately after the insult. • Intravascular contrast enhancement, another sign of early stroke (Figure 1f). • Sulcal effacement, gyral edema (Fig. 5b), loss of gray-white matter interface can occur within 12 hours of stroke. • Parenchymal contrast enhancement (Fig. 6d), mass effect (Fig. 4b) and hemorrhage can occur within 1-7 days of insult. Subacute infarct: (1 week to 8 weeks) • Contrast enhancement slowly decreases in time but can persist for 8 weeks, with decreasing mass effect and abnormal signal intensity: Old Infarct: •Focal area of encephalomalacia •Porencephalic dilatation of adjacent ventricle. • Residual old blood products may be present.
  • 18.
  • 19. conclusion • There are sequence of events in cerebral strokes : - Hyperacute - Acute - Subacute - Chronic • CT is best for hemorrhagic • MRI is best to detect the ischemic at the onset